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Manganese neonates

Deficiency of manganese may lead to vitamin K deficiency (Chiswell and Johnson 1994) and to problems in prenatal and neonatal development of the brain. [Pg.203]

The essentiality of manganese (Mn) for animals was established in 1931 by Orent and McCollum (1) who reported that this element is required for normal reproduction in the rat, and Kemmerer and colleagues (2) who showed that it was necessary for normal growth and reproduction in the mouse. Since then several investigators have verified the critical need of this nutrient for normal development (3). Manifestations of perinatal Mn deficiency in experimental animals include neonatal death, impaired growth, skeletal abnormalities, depressed reproductive function, congenital ataxia, and defects in protein, carbohydrate and lipid metabolism. [Pg.56]

Manganese deficiency results in a wide variety of structural, physiological and biochemical defects, for it has been implicated in a number of metabolic and enzymatic processes (5-15). Hurley has summarized the evidence that manganese is essential for normal prenatal and neonatal development, with deficiency resulting in a variety of congenital malformations (16). [Pg.68]

Two conclusions which could have practical importance may be derived so far 1) in combating neonatal iron deficiency, by increasing simultaneously iron and manganese content in milk it might be possible to diminish the risk of manganese deficiency and 2) milk does not seem to be the best means of additional nutrition in exposure to manganese. [Pg.72]

In a series of neonates on total long-term parenteral nutrition, cholestatic disorders were associated with high manganese concentrations (over 360 nmol/1) (21). [Pg.2202]

Synthetic tin protoporphyrin is a specific inhibitor of heme oxygenase and reduces plasma bilirubin concentrations in both adults and neonates, thereby preventing jaundice (1-3). A variety of heme analogues, such as tin, zinc, chromium, and manganese metalloporphyrins, act by competitive inhibition of cleavage of heme to biliver-din and carbon monoxide. Stannic porphyrins seem to be the most effective. The adverse effects are few, with only occasional erythema attributable to the phototoxicity of the metalloporphyrins. [Pg.2268]

Fok TF, Chui KK, Cheung R, Ng PC, Cheung KL, Hjelm M. Manganese intake and cholestatic jaundice in neonates receiving parenteral nutrition a randomized controlled study. Acta Paediatr 2001 90(9) 1009-15. [Pg.2721]

Cawte J Psychiatric sequelae of manganese exposure in the adult, foetal and neonatal nervous systems. Aust N Z J Psychiatry 19 211-217, 1985... [Pg.153]

A study measuring the retention of a single oral dose of radiolabeled manganese in adult and neonatal rats indicated that retention of the label 6 days after exposure was much greater in pups (67%) than in adults (0.18%) the addition of manganese to the animals drinking water decreased radiolabel retention in pups and adults (Kostial et al. 1989). [Pg.216]

Acute manganese exposure in drinking water was found to alter brain regional manganese levels in neonatal rats after 5 days of exposure, the highest level was in the striatum (12.05 pg/g wet weight) and... [Pg.216]

Similar transient body weight decreases and increases in motor activity were observed in neonatal rats administered 22 mg manganese (as MnCl2)/kg/day, by mouth or gavage, for up to 49 days (Brenneman et al. 1999 Dorman et al. 2000). [Pg.303]


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See also in sourсe #XX -- [ Pg.257 ]




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